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. 2020 Feb 27;11:323. doi: 10.3389/fimmu.2020.00323

FIGURE 4.

FIGURE 4

The crosstalk between Hippo-YAP pathway and NF-κB signaling. MST1/2 is activated via TLR2-MyD88-IRAK1/4 cascade during Mtb infection (a), and subsequently induce the expression of CXCL1 and CXCL2 by activating IRF3 (b). MST1 inhibits NF-κB activation via promoting IRAK1 degradation (c) and inhibiting LUBAC-mediated NEMO linear ubiquitination (d). MST1 is activated by TRAF2 after TNFα stimulation. NDR1 promotes the IL-17-induced inflammatory response by interact with TRAF3, which disrupts the IL-17R-Act1-TRAF6 complex (e). NDR1/2 inhibit inflammatory cytokine production by promoting Smurf1-mediated degradation of MEKK2 (f). YAP blocks NF-κB activation via promoting the TRAF6 degradation (g) or disrupting the interaction between TAK1 and IKKα/β (h). YAP/TAZ-TEADs complex inhibits the transcriptional activation of NF-κB targeted genes in low-density-cells (i). Long-term expression of YAP/TAZ in hepatocyte potently activates the expression of inflammatory factors (j). TNFα stimulation activates MST1 in a TRAF2 dependent manner (k). TAK1 directly phosphorylates YAP/TAZ, resulting in their degradation independent of LATS1/2 (l). MAP4K1 (m) and MAP4K3 (n) phosphorylate CARMA1 and PKC-θ, respectively, contributing to IKK and NF-κB activation. The crosstalk between Hippo-YAP and NF-κB signaling are highlighted with red color.